Tuberculous pericarditis pathophysiology

	Tuberculous pericarditis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Tuberculous pericarditis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Tuberculous pericarditis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Tuberculous pericarditis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Tuberculous pericarditis pathophysiology
CDC on Tuberculous pericarditis pathophysiology
Tuberculous pericarditis pathophysiology in the news
Blogs on Tuberculous pericarditis pathophysiology
Directions to Hospitals Treating Psoriasis
Risk calculators and risk factors for Tuberculous pericarditis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Pathophysiology

Pathogenesis

Tuberculous pericarditis develops as a result of lymphatic spread from peritracheal, peribronchial or mediastinal lymphnodes or by contiguous spread from a focus of infection in the lung or pleura. This causes acute inflammation of the pericardium with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may lead to pericardial effusion and fibrinous changes of the pericardium. There are four pathologic stages of involvement:^[1]^[2]^[3]

Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium

Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells

Stage 3: Absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.

Stage 4: Development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue.

Effusive constrictive pericarditis^[4] may be seen in some patients. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis) and concomitantly there is presence of pericardial effusion which may present as cardiac tamponade. In this scenario, the diastolic pressure continues to be elevated after pericardiocentesis due to persistent pericardial constriction.

Genetics

Associated Conditions

Gross Pathology Images

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Tuberculous pericarditis: Gross, natural color, shaggy hemorrhagic exudate. This case is much more hemorrhagic than the typical tuberculous pericarditis.

Microscopic Pathology Images